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The definitions for SIRS and sepsis can also be used to describe a disease continuum with respect to the severity of the illness.

Septic shock is a subset of severe sepsis. Note that current definitions have dropped the term ‘septicemia’ that may still be found in older textbooks. Bacteremia is the term for when organisms are cultured from blood.

Society of Critical Care Medicine (SCCM), European Society of Intensive Care Medicine (ESICM), The American College of Chest Physicians (ACCP), the American Thoracic Society (ATS), and the Surgical Infection Society (SIS)

An updated consensus conference still agreed that the concept of SIRS and sepsis was valid and useful. But expansion of the framework was needed to account for new knowledge and a broader approach to measurement of physiologic response (I.e. not restricted to just the 4 SIRS criteria). The presence of infection, response and organ dysfunction thus still defines severe sepsis. The central part of the diagram could also be labelled with ‘severe SIRS’ if the insult is not infectious.

Various innate factors are now known to have independent effects on the risk for sepsis and the outcome.

These clinical and laboratory markers of inflammation have all been associated with SIRS or sepsis. Procalcitonin is claimed to have reasonable diagnostic value for infection. Combinations of response markers may also be able to distinguish between sepsis and SIRS.

18.
• Infection: A microbial phenomenon characterized by an inflammatory response to the presence of microorganisms or the invasion of normally sterile host tissue by those organisms.• Bacteremia: The presence of viable bacteria in the blood.

22.
• Septic Shock: Sepsis induced with hypotension despite adequate resuscitation along with the presence of perfusion abnormalities which may include, but are not limited to lactic acidosis, oliguria, or an acute alteration in mental status.

23.
• Multiple Organ Dysfunction Syndrome (MODS): The presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.

45.
• Decreased red cell deformability in inflammatory states.• Microvascular sequestration of activated leukocytes and platelets.• Sepsis is a Procoagulant State. • The extrinsic pathway may be activated in sepsis by upregulation of Tissue Factor on monocytes or endothelial cells. • Fibrinolysis appears to be inhibited in sepsis by upregulation of Plasminogen Activator Inhibitor. • A variety of pathways result in reduced Protein C activity in sepsis.

46.
• Endothelial cell expression of Selectins and ICAM / ELAM is upregulated in Sepsis due to inflammatory activation. • Selectins bind carbohydrate ligands on the surfaces of PMN’s. • ICAM bind Integrins on the surfaces of PMN’s. • The Selectins initiate a weak bond between the PMN and the endothelial cell causing PMN’s to tumble along the vessel wall.

47.
• Binding of leukocytes to ICAM leads to transmigration of PMN’s into interstitium.• Transmigration disrupts normal cell-cell adhesions resulting in increased vascular permeability and tissue edema.• Vascular permeability is also increased by several types of inflammatory cytokines.

48.
• A physiologic process of homeostatically- regulated programmed cell death to eliminate dysfunctional or excessive cells.• A number of inflammatory cytokines, NO, low tissue perfusion, oxidative injury, LPS, and glucocorticoids all are known to increase apoptosis in endothelial and parenchymal cells.• Levels of circulating sfas (circulating apoptotic receptor) and nuclear matrix protein (general cell death marker) are both elevated in MODS.